Smoking a single cigarette does not produce a measurable reduction in brain MAO B in non-smokers

J. S. Fowler, G. J. Wang, N. D. Volkow, D. Franceschi, J. Logan, N. Pappas, C. Shea, R. R. MacGregor, V. Garza

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37 Scopus citations


Positron emission tomography (PET) studies with [11C]L-deprenyl-D2 have shown that brain monoamine oxidase (MAO) B is 40% lower in smokers than in non-smokers. Here we investigated whether MAO B inhibition can be detected after smoking a single cigarette. Eight normal healthy non-smokers (35 ± 11 years) received two PET studies 2 h apart with [11C]L-deprenyl-D2, one at baseline and the second 5-10 min after the subject had smoked a single cigarette. Plasma nicotine and expired carbon monoxide (CO) were measured prior to smoking and 10 min after smoking completion as an index of tobacco smoke exposure. A three-compartment model was used to calculate λk3, a model term which is proportional to MAO B activity and which is derived from the time course of carbon-11 in the brain and the time course of the radiotracer in the plasma and K1, the plasma-to-brain transfer constant (for [11C]L-deprenyl-D2) which is related to brain blood flow. Subjects experienced difficulty inhaling and became dizzy and/or nauseous after smoking. Plasma nicotine averaged 11.6 ± 5.5 ng/ml and expired CO averaged 8 ± 10 ppm after smoking. The average λk3 and K1 for 11 different brain regions did not differ significantly between baseline and smoking. These results indicate that the reduction in MAO B in smokers probably occurs gradually and requires chronic tobacco smoke exposure.

Original languageEnglish
Pages (from-to)325-329
Number of pages5
JournalNicotine and Tobacco Research
Issue number4
StatePublished - 1999
Externally publishedYes


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